Although most extrahepatic cells continuously acquire cholesterol as a result of the endocytosis and lysosomal hydrolysis of plasma low-density lipoproteins (LDL), only those endocrine cells which synthesize steroid hormones are able to ‘dispose’of it by oxidation. Hepatocytes differ from peripheral cells in being able to eliminate cholesterol from the body via the bile, both as cholesterol itself (0.3-1. O g/day) and after conversion to the primary bile acids, cholic acid and chenodeoxycholic acid (0.1-0.4 g/day). Cholesterol is also a component of lipoproteins that are secreted into the circulation by hepatocytes. These include the triglyceride-rich very-lowdensity lipoproteins (VLDL), which are subsequently converted to LDL through the action of endothelium-bound lipases. From these considerations it will be clear that there must be a continuous bi-directional flux of cholesterol between hepatocytes and peripheral cells. Movement of cholesterol from the periphery to hepatocytes is usually referred to as ‘reverse cholesterol transport’. We will review the experimental evidence and some current hypotheses concerning the different components of this process, and discuss them in the light of observations made in man.